Signaling Pathways in Endometriosis (Eutopic/Ectopic)

Yin, Xunqin

doi:10.1002/9781444398519.ch16

Cited by 3 publications

(2 citation statements)

References 81 publications

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“…This pathway regulates fundamental cellular functions, such as cell proliferation, cell growth, and apoptosis in response to many types of stimuli (inflammation, toxicants, etc.) [ 51 ]. In endometriosis, some studies, including our own, suggest upregulation of AKT1, which may cause induction of the AKT signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

The Eutopic Endometrium Proteome in Endometriosis Reveals Candidate Markers and Molecular Mechanisms of Physiopathology

et al. 2022

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Endometriosis is a common chronic gynaecological disease causing various symptoms, such as infertility and chronic pain. The gold standard for its diagnosis is still laparoscopy and the biopsy of endometriotic lesions. Here, we aimed to compare the eutopic endometrium from women with or without endometriosis to identify proteins that may be considered as potential biomarker candidates. Eutopic endometrium was collected from patients with endometriosis (n = 4) and women without endometriosis (n = 5) during a laparoscopy surgery during the mid-secretory phase of their menstrual cycle. Total proteins from tissues were extracted and digested before LC-MS-MS analysis. Among the 5301 proteins identified, 543 were differentially expressed and enriched in two specific KEGG pathways: focal adhesion and PI3K/AKT signaling. Integration of our data with a large-scale proteomics dataset allowed us to highlight 11 proteins that share the same trend of dysregulation in eutopic endometrium, regardless of the phase of the menstrual cycle. Our results constitute the first step towards the identification of potential promising endometrial diagnostic biomarkers. They provide new insights into the mechanisms underlying endometriosis and its etiology. Our results await further confirmation on a larger sample cohort.

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Section: Discussionmentioning

confidence: 99%

The Eutopic Endometrium Proteome in Endometriosis Reveals Candidate Markers and Molecular Mechanisms of Physiopathology

et al. 2022

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“…thus, resistance to P 4 and progestins can have a major impact on pain relief, disease control and fertility success of affected women. Several signaling pathways have been implicated in these aspects of the pathophysiology of progesterone resistance and compromised stromal fibroblast decidualization, including protein kinase A (PKA), mitogen-activated protein kinase (MAPK), and phosphatidylinositide-3 kinase/AKt/ mammalian target of rapamycin (PI3K/AKt/mtOR) (8). Understanding involvement and cross-talk among these pathways, and whether pathway-specific inhibitors can restore endometrial cell function or biomarkers, is of great interest as they hold promise to mitigate endometrial cellular dysfunction in the setting of disease.…”

Section: Human Endometrial Samplesmentioning

confidence: 99%

Inhibition of epidermal growth factor receptor restores decidualization markers in stromal fibroblasts from women with endometriosis

Erikson

Chen

Piltonen

et al. 2014

Journal of Endometriosis and Pelvic Pain Disorders

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Purpose Decidualization comprises specific biochemical and morphological changes in uterine endometrium essential for establishment of pregnancy. This process is abnormal in women with endometriosis, a disorder in which endometrial-like tissue is present outside the uterus. The aim of this study was to restore cAMP-induced decidualization marker expression in endometrial stromal fibroblasts from women with endometriosis by using chemical inhibitors to PI3K/AKT/mammalian target of rapamycin (mTOR), mitogen-activated protein kinase (MAPK) and epidermal growth factor receptor (EGFR) signaling pathways in vitro. Methods Endometrial stromal fibroblasts (eSF) from women with (eSFendo) and without (eSFnon-endo) endometriosis were treated with inhibitors to EGFR tyrosine kinase (gefitinib), mTOR (rapamycin) and MAPK kinase 1/2 (MEK1/2) (UO126) during 8-bromoadenosine 3′,5′-cyclic monophosphate (8-br-cAMP)–stimulated decidualization. Decidualization was assessed by evaluating expression of insulin growth factor binding protein 1 (IGFBP1), prolactin (PRL) and forkhead box protein O1A (FOXO1A) by quantitative real-time PCR. Results Gefitinib restored expression of decidualization markers in eSFendo to levels consistent with those in eSFnon-endo. Elevated levels of phosphorylated mTOR in eSFendo were reduced to levels found in eSFnon-endo, by gefitinib during treatment with 8-br-cAMP. Additional gene expression analyses suggested dysregulation of EGFR negative feedback regulators in eSFendo. Conclusions Results implicate EGFR signaling as an underlying cause for aberrant cAMP-induced decidualization in women with endometriosis, and provide a potential target for management of infertility associated with the disease. The reduction of p-mTOR levels in eSFendo during 8-br-cAMP treatment suggests cooperation between EGR and protein kinase A signaling in the regulation of mTOR in eSF.

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Influence of AKT on Progesterone Action in Endometrial Diseases

Lee

Kim

2014

Biology of Reproduction

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Progesterone plays an essential role in the maintenance of the endometrium; it prepares the endometrium for pregnancy, promotes decidualization, and inhibits estrogen-dependent proliferation. Progesterone function is often dysregulated in endometrial disease states. In addition, the PI3K/AKT signaling pathway is often overactive in endometrial pathologies and promotes the survival and proliferation of the diseased cells. Understanding how AKT influences progesterone action is critical in improving hormone-based therapies in endometrial pathologies. Here, we summarize recent studies investigating the crosstalk between the AKT pathway and progesterone receptor function in endometriosis and endometrial cancer.

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Signaling Pathways in Endometriosis (Eutopic/Ectopic)

Cited by 3 publications

References 81 publications

The Eutopic Endometrium Proteome in Endometriosis Reveals Candidate Markers and Molecular Mechanisms of Physiopathology

The Eutopic Endometrium Proteome in Endometriosis Reveals Candidate Markers and Molecular Mechanisms of Physiopathology

Inhibition of epidermal growth factor receptor restores decidualization markers in stromal fibroblasts from women with endometriosis

Influence of AKT on Progesterone Action in Endometrial Diseases

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